NLRP3 Inflammasome: A key contributor to the inflammation formation.

Food Chem Toxicol

Henan Key Laboratory of Immunology and Targeted Drugs, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, 453003, Henan, PR China. Electronic address:

Published: April 2023

Inflammation is an important part of the development of various organ diseases. The inflammasome, as an innate immune receptor, plays an important role in the formation of inflammation. Among various inflammasomes, the NLRP3 inflammasome is the most well studied. The NLRP3 inflammasome is composed of skeletal protein NLRP3, apoptosis-associated speck-like protein (ASC) and pro-caspase-1. There are three types of activation pathways: (1) "classical" activation pathway; (2) "non-canonical" activation pathway; (3) "alternative" activation pathway. The activation of NLRP3 inflammasome is involved in many inflammatory diseases. A variety of factors (such as genetic factors, environmental factors, chemical factors, viral infection, etc.) have been proved to activate NLRP3 inflammasome and promote the inflammatory response of the lung, heart, liver, kidney and other organs in the body. Especially, the mechanism of NLRP3 inflammation and its related molecules in its associated diseases remains not to be summarized, namely they may promote or delay inflammatory diseases in different cells and tissues. This article reviews the structure and function of the NLRP3 inflammasome and its role in various inflammations, including inflammations caused by chemically toxic substances.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.fct.2023.113683DOI Listing

Publication Analysis

Top Keywords

nlrp3 inflammasome
24
activation pathway
12
nlrp3
8
formation inflammation
8
inflammatory diseases
8
inflammasome
6
activation
5
inflammasome key
4
key contributor
4
inflammation
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!